Ftplectures fluids/Electrolytes system Lecture Notes

FLUIDS
&
ELECTROLYTES

Medicine made simple

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Ftplectures Clinical Medicine
Copyright 2014

Adeleke Adesina, DO
Clinical Medicine

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Fluid and electrolytes introduction
Objectives of learning
Normal body fluid compartments
Normal intake of water
Normal output of water
Insensible water loss
Assessment of fluid volume

Normal body fluid compartments

Male total body water = 60% of the body weight
Female total body water = 50% of the body weight
The body fluid is divided into two compartments:
1. Intracellular fluid compartment (2/3 of total body water)
2. Extracellular fluid compartment (1/3 of total body water)
Extra cellular fluid compartment is further divided into interstitial compartment (3/4 of
extracellular fluid) and blood vessels (1/4 of extracellular fluid)

Total  body  fluids  

plasma  
8%  

Inters//al  
25%  

Intracellular  
67%  

Intracellular   Inters//al   plasma  

Normal input of water
Total average input of water = 2000ml
1500ml oral intake + 500ml solids = 2000ml

Normal output of water

Urine output = 800-1500ml
Stool output = 250ml

Minimum urine output should be 500-600 ml per day.

Insensible water loss

Total insensible water loss is 600-900 ml.
Sweating (varies according to external environment and occupation)
Fever (for every 1 degree raise in temperature above 37 degree Celcius there is
100ml/day water loss.)
Hyperventilation (carbon dioxide and water are excreted)

Assessment of fluid volume

Dry mucous membranes and poor skin turgor
Input/output
Urine output (normal output 1ml/kg/hour)
Sodium and Water regulation
Objectives of learning
Role of kidneys
Water reabsorption
Sodium reabsorption
Sodium regulation
Water regulation

Role of kidneys
Glomerulus has afferent and efferent capillaries producing GFR (glomerular filtration
rate).
Proximal convoluted tubules reabsorb most of the sodium.
Thick ascending loop of Henle absorb sodium actively.
Distal convoluted tubule reabsorb remaining sodium.
Collecting tubules are under direct influence of aldosterone which reabsorb more
amount of sodium in the ECF.

Water reabsorption
Water moves according to the levels of sodium. Where sodium is present in higher
quantities, it draws more and more water. Thus, sodium determines the extracellular
fluid compartment.

Sodium reabsorption
Sodium determines the amount of extracellular fluid.
When there is hypervolemia, there is increased sodium levels in the extracellular fluid.
The causes are parenteral over hydration, cirrhosis, renal failure and congestive heart
failure
When there is hypovolemia, there is decreased sodium levels in the extracellular fluid.
The causes are inadequate drinking, vomiting, diarrhea, small bowel obstruction, NG
tube suction, diabetic ketoacidosis, third spacing i.e. effusions, ascites and burns.
Sodium regulation
Juxtaglomerular apparatus
Volume receptors
Sympathetic nervous system

Water regulation
The water is regulated by the factors that are shown in the following equation

Osmolality = 2 Na + Glucose/18 + BUN/2.8

When plasma osmolality is >295, then hypothalamus stimulates the thirst center.
Osmolality and tonicity
Osmolality
The total amount of solute in fluid compartment is called osmolality.

The important solutes are sodium, glucose and urea.

According to formula:

Osmolality = 2(Na) + Glu/18 = BUN/2.8

The normal serum osmolality ranges from 280-295.

From the above equation it is quite clear that sodium is the main component which determines
plasma osmolality. Glucose also affects the osmolality e.g. in hyperglycemia, the excess
glucose draws more and more blood into the extracellular fluid from intracellular fluid. The
intracellular fluid moves out of the cell and is responsible for polydipsia. Urea, on the other hand,
has ability to move freely inside and outside of the cell. So it has less effect on the plasma
osmolality.

Tonicity
The combined effect of solutes in extra cellular compartment to cause water to move from one
compartment to another compartment across the semi permeable membrane.

For example, if sodium concentration in the blood is increased then plasma osmolality is also
raised and the solution is hypertonic. This solution has tendency to draw more and more water
from the intracellular fluid compartment into the extracellular fluid compartment.

In contrast, if sodium concentration is decreased then plasma osmolality is also decreased and
the solution if hypo tonic. This solution has tendency to move into the intracellular compartment
and causing swelling of the cell.

Isotonic solution has equal concentration of solutes in the intracellular and extracellular fluid
compartment.
Hypervolemia
Objectives of learning
Definition
Causes
Pathophysiology
Clinical features
Physical examination
Treatment and management

Definition
Increased total body volume i.e. more than 60% is called hypervolemia.

Causes
Parenteral over hydration
Cirrhosis
Renal failure
Congestive heart failure

Pathophysiology
The pathophysiology behind congestive heart failure, cirrhosis and renal failure is the
decreased renal perfusion which activates the rennin-angiotensin-aldosterone pathway.
Aldosterone reserves the sodium which attracts water into the extra cellular fluid
compartment and thus makes the serum hypervolemic.

Clinical features
Weight gain
Jugular venous distention
Ascites
Pulmonary edema
Peripheral edema
Physical examination
Pulmonary rales
Elevated central venous pressure and pulmonary capillary wedge pressure
Diagnosis
Decreased hematocrit
Low albumin especially in cirrhosis and nephrotic syndrome

Treatment and management

Fluid restriction
Loop diuretic i.e. furosemide
Monitor urine output and weight of the patient till complete recovery
Hypovolemia

Objectives of learning
Definition
Clinical presentation
Diagnosis
Treatment

Definition
Less than normal body fluid volume of 60% is called hypovolemia.

Causes
Inadequate drinking
Vomiting
Diarrhea
Small bowel obstruction
NG tube suction
Diabetic ketoacidosis
Third spacing i.e. effusions, ascites and burns
Skin (75% water)
Lungs (25% water)
Trauma i.e. hemorrhage, open wounds

Clinical presentation
Central nervous system effects
Cardio vascular effects i.e. Low blood pressure, tachycardia, feeble but rapid pulse,
orthostatic hypotension
Poor skin turgor i.e. dry skin
Oliguria i.e. low urine output
Acute renal failure

Diagnosis
Urinary output measurement
Daily weight
Central venous pressure
Pulmonary capillary wedge pressure
Serum sodium level (elevated)
Urinary sodium level (decreased)
Hematocrit is usually raised up to 3%

Treatment
Correct volume of blood using normal saline, ringer lactate
Maintain urine output 0.5-1 ml/kg/hr
Maintenance fluid should be given comprising of Dextrose 50g, 0.45% normal saline
and add 20 mEq potassium chloride.
Hyponatremia
Objectives of learning
Definition
Symptoms
Signs
Diagnosis
Treatment and
Management

Definition
Low sodium level in the blood is hyponatremia i.e. less than 135 mEq/L
Symptoms of hyponatremia appear when sodium level is less than 120 mEq/L

Approach to hyponatremia
Before going in detail of hyponatremia, one should be well aware of plasma osmolality.
Plasma osmolality = 2(Na) + Glucose/18 + BUN/1.8 (Normal = 280-295 mOsm/L)
According to the above formula, the plasma osmolality can be affected by sodium,
glucose or blood urea nitrogen levels.
If the person is suffering from hyponatremia, then he may have normal, high or low
osmolality depending on the aggregate of all the three basic factors.
In hypertonic hyponatremia (plasma osmolality greater than 295), there is increased
level of glucose, sorbitol or mannitol in the blood and they attract greater amount of
water. Thus hyponatremia ensues.
In pseudo hyponatremia (normal plasma osmolality between 280-295), there are
elevated plasma proteins (multiple myeloma), hypertriglyceridemia i.e. more than 1000
mg/dl or excess of D5W i.e. 5% Dextrose water.
In true hyponatremia (plasma osmolality less than 280), this low level of sodium may
be associated with hypervolemia, hypovolemia or normal volume. The causes of
hypervolemia are congestive heart failure, nephrolithiasis and cirrhosis. The cause of
hypovolemia is mainly renal excretion of sodium as in diuretics, poisoning and acute
tubular necrosis. There are conditions, in which urine secretion of sodium is low i.e. less
than 10, like diarrhea, vomiting and third spacing. In patients with normal plasma
volume, there can be SIADH, hypothyroidism, psychogenic polydipsia or post operation.
Symptoms and signs
CNS symptoms are predominant due to cerebral swelling, edema which manifest
themselves in the form of headache, delirium, irritability, hyperactive deep tendon reflex,
weakness, muscle twitching and raised intra cranial pressure culminating into seizures
and coma.
CVS symptoms include hypertension due to raised intra cranial pressure
GI symptoms may include nausea, vomiting
Renal symptoms include oliguria, anuria

Diagnosis
Calculate plasma osmolality by using formula:
2 Na + glucose/18 + BUN/2.8 (normal range 280-295)
If plasma osmolality is normal or greater than 295 then the patient must have elevated
glucose or BUN.
If plasma osmolality is less than 280 then the patient is truly hyponatremic hypo osmolar
Urine osmolality
If urine osmolality is less than normal, then person is having primary polydipsia.
If urine osmolality is greater than normal, then the person is suffering from SIADH,
dehydration, hypothyroidism or CVS failure.

Treatment and management

In isotonic hyponatremia (pseudohyponatremia), just treat the underlying cause i.e.
multiple myeloma and triglyceridemia
In hypertonic hyponatremia, there is elevated glucose level. So giving insulin along with
fluids and potassium should treat the patient.
In true hyponatremia, there are three cases:
If sodium levels are between 120-130, then holding the free water will cure the patient
If sodium levels are between 110-120, then normal saline with loop diuretic will cure the
patient
If sodium levels are below 110, then IV hypertonic solution will cure the patient. The
hypertonic solution should be given at the rate of 1-2 mEq per hour. If IV fluid rate is
much faster than recommended dose, the brain will suffer from a condition called
“central pontine demyelination”.

 
Hypernatremia

Objectives of learning
Definition

Causes

Types of hypernatremia

Clinical features

Diagnosis

Treatment and management

Complication

Definition
Elevated amount of sodium inside blood i.e. more than normal 135-145 mEq/L is called
hypernatremia.

Causes
Too much infusion containing sodium ions

Eating too much salty food

Underlying pathology

Types of hypernatremia
There are three types of hypernatremia:

1. Hypovolemic hypernatremia
2. Isovolemic hypernatremia
3. Hypervolemic hypernatremia

Hypovolemic hypernatremia Isovolemic hypernatremia Hypervolemic hypernatremia

There is water loss Normal water level There is gain of water

Renal loss i.e. diuretics,
diabetes
Extrarenal loss i.e. diarrhea,
diaphoresis
Diabetes insipidus is Iatrogenic cause i.e. infusion
common cause of sodium bicarbonate
Insensible respiratory loss i.e. Cushing syndrome
tachypnea
Exogenic steroids
 Primary hyperaldosteronism

Clinical features
CNS effects are altered mental status, focal neurologic deficits, seizures, confusion leading to
coma

Tissue effects are dry, thick mucus membranes, thick saliva

Diagnosis
Urine output should be monitored for renal functions

Urine osmolality may be greater than 380 mOsm/L

Desmopressin test for differentiating between central and nephrogenic diabetes

Treatment and management

Hypovolemic hypernatremia Isovolemic hypernatremia Hypervolemic hypernatremia

Give isotonic NS Give vasopressin Give diuretics i.e. furosemide

Stop diuretics Diabetes insipidus patients 5% dextrose water

are treated by this drug

Control diabetes Oral fluids

5% dextrose water

Complication
Rapid correction of hypernatremia will lead to cerebral edema. Rate of sodium correction should
not exceed > 12 mEq/L or less than 8 mEq/L
Potassium regulation
Objectives of learning
Location of potassium
Functions
Sources
Excretion
Regulation
Factors increasing potassium secretion

Location
Potassium is present inside the cells. It is most common cation present in human cells.
Sodium-potassium ATPase pump is responsible for maintaining the high quantities of
potassium within the cell.
The intracellular concentration of potassium is very high but we are concerned with
extracellular potassium i.e. 3.5-5 mEq/dL

Functions of potassium
Cardiac rhythm i.e. SA node, Purkinje fibers, AV node
Cellular function
Neurovascular transmission

Sources
Diet
Skeletal muscles (lysis of muscles)
RBCs (lysis of RBC)
GI bleed
KCl injection

Potassium excretion
90% potassium is excreted through kidneys
10% potassium is excreted in feces
Potassium regulation
Thick ascending loop of Henle bears NaK2Cl transporter that reabsorb most of the
sodium, potassium and chloride.
Collecting tubules are acted upon by aldosterone. Aldosterone helps in reabsorption of
sodium while excreting potassium into the lumen of tubules.

Factors increasing potassium excretion

Increased aldosterone i.e. hyperaldosteronism
Increased delivery of sodium to collecting ducts i.e. diuretics furosemide,
hydrochlorothiazide
Metabolic alkalosis i.e. greater amount of bicarbonates draw more sodium with it
delivers the excess of sodium to the collecting ducts
DKA diabetic ketoacidosis patients have polyuria. As more and more water is excreted
out, there is dehydration and decreased perfusion of the glomerulus. Thus, rennin-
angiotensin system is activated and aldosterone concentration is increased which act
on collecting tubule.
Hyperkalemia
Objectives of learning
Definition
Etiology
Clinical features
Treatment

Definition
Increase serum potassium levels i.e. more than normal 3.5-5.0 mEq/L is hyperkalemia.

Etiology
Acute/chronic renal failure
Spurious causes:
Lab errors
Hemolysis in the test tube
Thrombocytosis
Leukocytosis
Prolong tourniquet
Redistribution of potassium:
Metabolic acidosis results in exchange of hydrogen ions with potassium
Insulin deficiency especially in diabetes mellitus
Drugs i.e. digitalis, beta blockers, succinylcholine
Rhabdomyolysis
GI bleed
Conditions causing low aldosterone level
Hyporennin hypoaldosteronism syndrome
Addison’s disease
ACE inhibitors

Clinical features
The clinical features start appearing when potassium levels are more than 6 mEq/L and
include
Arrhythmia
Muscle weakness, paralysis,
Decreased deep tendon reflex
Respiratory failure
Diarrhea
Nausea
Vomiting

Treatment
Calcium gluconate, calcium chlodride are given. But it increases digitoxin toxicity
Beta agonist i.e. albuterol
Insulin with glucose
Kayexalak, a sodium-potassium resin
Dialysis
Hypokalemia
Objectives of learning
Definition
Causes
Clinical features
Diagnosis
Treatment

Definition
Potassium levels of less than normal 3.5-5.5 mEq/L is termed as hypokalemia.

Causes of hypokalemia
Renal losses:
Normally, 90% of potassium is excreted through kidneys. The excess potassium is
excreted by the kidneys in cases of diuretics (furosemide, thiazide), renal tubular
acidosis, hyper aldosteronism, hypomagnesemia, Batter’s syndrome
Extra renal losses (GI loss):
Diarrhea
Vomiting
Laxatives
Other causes
Poor diet intake
Insulin
Profuse sweating
Antibiotics I.e. gentamicin, cisplatin, penicillin, theophylline and epinephrine

Clinical features
Arrhythmia
Muscle weakness, fatigue, paralysis or cramps
Worsen digitalis toxicity

Diagnosis
Serum electrolytes
Urine potassium concentration
Treatment
Treating the original cause of hypokalemia will cure the patient
Oral KCl is given in patients with moderately low potassium level
IV KCl is given in severely hypokalemic patients with great care
Hypercalcemia
Objectives of learning
Definition
Normal metabolism of calcium
Causes
Clinical features
Treatment and management

Definition
Hypercalcemia is the elevated calcium level in the blood.

Normal metabolism of calcium

80% of ingested calcium is removed in the feces
2% of calcium is reabsorbed
Out of all the calcium levels in the blood:
50% is free calcium ion in the plasma
40% is the protein bound calcium
10% is the citrate/phosphate bound

Causes
Hyperparathyroidism is the most common cause
Neoplasms are second most common cause e.g. small cell carcinoma of lung

Calcium intake
Hyperparathyroidism/ hyperthyroidism
Iatrogenic i.e. thiazide diuretic
Mumps
Paget’s disease of the bone
Acidosis
Neoplasm
Zollinger-Ellison syndrome
Excess vitamin D
Excess vitamin A
Sarcoidosis
Clinical features
CNS: Altered mental status, lethargic and confusion
Renal: Nephrolithiasis, diabetes insipidus
GI: Constipation, pancreatitis
CVS: tachycardia, decreased QT interval

Treatment and management

IV fluids
Diuretics i.e. furosemide
Bisphosphonates
Calcitonin